The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway serves as a core signaling axis for sensing cytosolic DNA and activating innate immunity. By recognizing abnormal DNA released from pathogens or tissue damage, it triggers the expression of type I interferons (IFN-I) and inflammatory cytokines, playing a pivotal role in innate immune defense, tumor immune surveillance, and tissue homeostasis regulation. As an important signaling hub in the fibroblast microenvironment, this pathway is involved in various pathophysiological processes such as antiviral immune responses, fibrosis progression, and remodeling of the tumor microenvironment (TME). In recent years, its potential in targeted therapy has become increasingly prominent: agonists of the pathway can enhance anti‑tumor immune responses, while inhibitors hold promise for alleviating aberrant inflammatory responses in fibrotic and autoimmune diseases. This review introduces the structural composition, signaling transduction process, and biological functions of the cGAS-STING pathway, and provides an overview of current research advances on related diseases, demonstrating the great potential of targeting this pathway in disease treatment.

Fibrosis is a pathological process characterized by the abnormal deposition of connective tissue across multiple organ systems. Given the high prevalence of fibrotic diseases and the limited availability of clinical treatment options, it has emerged as a major challenge in contemporary medicine. Chronic inflammation is widely recognized as a common pathological basis of various fibrotic disorders. In fibrosis progression, CCR2 acts as a critical signaling hub, initiating cascade reactions and contributing to the formation of a complex regulatory network. Studies have demonstrated that in most organ fibrotic processes, CCR2 primarily exerts pro-fibrotic effect by recruiting inflammatory monocytes, activating fibroblasts, and promoting extracellular matrix deposition. However, the function of CCR2 is not unidimensional. It may also play a regulatory role in promoting fibrosis regression under specific tissue and pathological contexts. CCR2 signaling exhibits dual regulatory properties at different stages of liver fibrosis. CCR2 promotes injury in the early phase, while participating in fibrosis reversal by mediating macrophage transition toward a reparative phenotype and facilitating extracellular matrix degradation. This stage-dependent behavior suggests that inappropriate timing of intervention may disrupt repair process, and the functional redundancy of the chemokine system may trigger compensatory adaptations. Together, these factors constitute the core translational challenges facing CCR2-targeted therapeutic strategies. This article systematically reviews the complex regulatory network and pivotal role of CCR2 signaling in fibrosis progression, summarizes the latest advances in the diagnosis and treatment of clinically relevant fibrotic diseases associated with this pathway, analyzes the specific challenges in translating CCR2-targeted therapies into clinical practice, and outlines future research directions.

This study highlights the role of moderate-to-vigorous physical activity (MVPA) in preventing degenerative aortic valve stenosis (AS). Using 7-day wrist-worn accelerometer data from the UK Biobank, researchers found that higher MVPA was associated with a lower risk of developing AS. Similar associations were observed using self-reported physical activity in a parallel cohort, providing additional validation. These results suggest that AS may be partly modifiable through lifestyle interventions and highlight the potential of activity metrics measured by wearable devices to guide preventive strategies.

Cardiac function has been found to be particularly vulnerable to climate change and temperature variability. However, the specific molecular mechanisms underlying the pathogenesis of heat stroke (HS)-induced myocardial dysfunction remain largely elusive. In this study, we constructed a cardiomyocyte-specific peroxisome proliferator-activated receptor γ (PPARγ) knockout mouse model subjected to HS to investigate the key role of PPARγ. RNA sequencing analysis was performed to identify downstream targets of PPARγ. Rosiglitazone, a PPARγ agonist, was examined for its therapeutic potential against HS-induced myocardial injury. Our results showed that HS significantly downregulated the expression of PPARγ. Cardiomyocyte-specific knockout of PPARγ exacerbated myocardial injury in mice subjected to HS. RNA-seq analysis revealed that differentially expressed genes were mainly enriched in lipid metabolism-related pathways, particularly ABC transporters. Further experiments demonstrated that ABCC5 serves as a pivotal downstream factor mediating the cardioprotective effects of PPARγ overexpression against HS. HS also led to the accumulation and deposition of lipids in the myocardium and serum over an extended period, which was partly attributed to the downregulation of the PPARγ/ABCC5 pathway. Importantly, we demonstrated that treatment with either rosiglitazone (a PPARγ agonist) or atorvastatin (a lipid-lowering drug) holds promising therapeutic potential for ameliorating HS-induced myocardial dysfunction. These findings indicate that PPARγ protects against HS-induced myocardial pathological manifestations through ABCC5-dependent regulation of lipid metabolism.

The neurotrophin receptor p75 (p75NTR) plays dual, context-dependent roles in the nervous system that are regulated by ligand binding, co-receptor interactions, and microenvironmental cues. During neurodevelopment, synaptic plasticity, and in neurodegenerative disorders, p75NTR orchestrates opposing cellular responses: it can support neuronal homeostasis through pro-survival pathways, while also initiating apoptotic and inflammatory cascades that exacerbate disease progression. In Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), activation of p75NTR drives pathological processes such as neuronal apoptosis and axonal degeneration, leading to impaired cognitive and motor function.Importantly, different structural domains of p75NTR have divergent effects. The extracellular domain (p75ECD) exhibits neuroprotective properties in AD models, in contrast with the pro-apoptotic activity associated with the full-length receptor. Therapeutic targeting of p75NTR with small-molecule ligands and ROCK inhibitors has shown efficacy in preclinical models, and some candidates have progressed to clinical trials. However, several challenges hinder clinical translation: (1) the mechanisms underlying p75NTR upregulation are not fully understood; (2) its downstream signaling network is highly complex; and (3) existing biomarker systems remain limited.A comprehensive understanding of p75NTR's role in neurodegeneration may clarify pathological mechanisms and reveal novel therapeutic targets. Achieving this will require multidisciplinary collaboration to bridge the gap between basic research and clinical applications.

Myocardial ischemia-reperfusion injury (MIRI) represents a major clinical challenge in cardiovascular therapy. The NLRP3 inflammasome plays a critical role in the pathogenesis of MIRI, yet the effect of Acteoside (Act) on NLRP3 inflammasome during MIRI remains unclear. Network pharmacology combined with molecular docking was employed to predict and validate the key targets and pathways underlying Act-mediated regulation of MIRI-related pyroptosis. For the in vivo study, a rat MIRI model was established via 30 min of left anterior descending coronary artery ligation followed by 2 h of reperfusion. Rats were randomly divided into four groups: the Sham group, the MIRI model group, the Act pretreatment plus MIRI group, and the Act pretreatment plus MIRI plus LY294002 (a PI3K inhibitor) group. For the in vitro assay, H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) and then treated with Act alone or in combination with LY294002. Cardiac function, myocardial infarct size, myocardial injury, histological alterations, and mitochondrial morphological changes were assessed. Oxidative stress, cardiomyocyte apoptosis, and the levels of inflammatory cytokines IL-1β and IL-18 were detected. The expression of NLRP3 inflammasome-related proteins and PI3K/Akt signaling pathway proteins were measured. Network pharmacology analysis identified the PI3K/Akt signaling pathway as a key mechanism mediating the effects of Act on MIRI. Molecular docking results confirmed that Act interacts with core components of the NLRP3 inflammasome, and that the NLRP3 inflammasome is associated with the PI3K/Akt pathway. Pretreatment with Act alleviated MIRI-induced myocardial injury, improved cardiac function and mitochondrial morphology, inhibited NLRP3 inflammasome activation, promoted the phosphorylation of PI3K/Akt, suppressed cardiomyocyte apoptosis and oxidative stress, and reduced the levels of IL-1β and IL-18. Notably, these protective effects of Act were partially reversed by LY294002. Act attenuates MIRI by inhibiting the NLRP3 inflammasome through activation of the PI3K/Akt signaling pathway, indicating its potential as a promising therapeutic agent for MIRI.

Emerging as a novel secreted protein, Meteorin-like (Metrnl) exhibits substantial sequence homology with Meteorin (Metrn). Although Metrnl was initially identified in the context of adipose tissue and metabolic regulation, accumulating evidence has demonstrated its widespread expression across multiple tissues, including the nervous system, barrier tissues, and skeletal muscle. Functionally, Metrnl exerts pleiotropic biological effects and has been implicated as an adipokine, an immunomodulatory factor, and a cytoprotective mediator. This review provides an overview of current knowledge regarding the tissue-specific actions of Metrnl and summarizes the major signaling pathways associated with its activity. The integral role of Metrnl across different systems in both health and disease states is further examined, with a focus on elucidating its pathological involvement in various human disorders.

This study aimed to explore whether Morin could improve postoperative cognitive dysfunction (POCD) by inhibiting hippocampal ferroptosis through miR-138-5p/SIRT1. Morin improves the cognitive function of POCD mice by inhibiting the expression of miR-138-5p and promoting the expression of SIRT1 protein. When detecting ferroptosis-related indicators (such as GSH, MDA, and iron ion levels), it was found that miR-138-5p agomir blocked the regulatory effect of Morin on these indicators. Protein detection showed that Morin regulated the ferroptosis process by controlling the miR-138-5p/SIRT1 axis to affect the expression of p53, SLC7A11, and GPX4. In vitro cell experiments showed that after Erastin induction, the GSH level in HT22 cells decreased, the MDA and Fe2+ contents increased, and the ROS fluorescence intensity increased; after Morin treatment, these oxidative stress indicators were significantly improved, the expression of SIRT1, SLC7A11 and GPX4 increased, and the expression of p53 decreased. The miR-138-5p mimic aggravated the upregulation of oxidative stress and the regulation of ferroptosis-related genes, while the miR-138-5p inhibitor had the opposite effect. Morin improved cognitive function and neuronal morphology in POCD mice by inhibiting miR-138-5p and upregulating SIRT1. It also inhibited ferroptosis through the miR-138-5p/SIRT1 pathway, further confirming its protective role in POCD.

BCL3 (B-cell CLL/lymphoma 3), initially identified in the t(14;19) chromosomal translocation in B-cell malignancies, is an atypical member of the inhibitor of NF-κB (IκB) protein family. Unlike classical IκB proteins, BCL3 predominantly localizes to the nucleus, where it exerts unique bidirectional transcriptional regulatory functions within the NF-κB signaling pathway. This complex functionality is finely modulated by post-translational modifications, particularly phosphorylation. Under pathological conditions, BCL3 functions as an oncogene, driving abnormal neoplastic cell proliferation, inhibiting apoptosis, and promoting metastasis and chemotherapy resistance in various hematological malignancies and solid neoplasms by activating multiple oncogenic signaling pathways. Conversely, BCL3 also serves as a critical regulatory factor of immune homeostasis, modulating the functions of macrophages, T cells, and dendritic cells (DCs), thereby influencing the pathogenesis of immune-related disorders. Beyond oncology and immunology, BCL3 plays pivotal roles in the nervous, cardiovascular, digestive, and musculoskeletal systems, highlighting its broad physiological and pathological significance. This article systematically reviews the molecular structure, post-translational regulatory mechanisms, and multifaceted roles of BCL3 in neoplastic and non-neoplastic diseases. By consolidating current research, this review aims to provide novel insights into the diagnostic and therapeutic potential of targeting BCL3 in related pathologies.

INTRODUCTION:Cardiovascular diseases (CVDs) pose a significant threat to the health of middle-aged and elderly people. They are widely recognized as a major public health concern. The sirtuin (SIRT) family comprises seven proteins (SIRT1-SIRT7), all of which contain a highly conserved nicotinamide adenine dinucleotide (NAD+)-binding catalytic domain. Notably, SIRT1 influences the development and progression of CVDs by regulating biological processes such as inflammation, immune responses, oxidative stress, and autophagy. AREAS COVERED:This review summarizes the biological functions of SIRT1 and its role in major cardiovascular conditions, with particular attention to cell-type-specific effects. It examines the preclinical efficacy of SIRT1 activators, such as resveratrol and SRT1720, and discusses challenges including dose dependency, specificity, and barriers to clinical translation. A comprehensive literature search (PubMed, Web of Science, Scopus; 2000-April 2026) was conducted to identify studies on SIRT1 in CVDs, with a focus on mechanistic insights and therapeutic relevance. EXPERT OPINION:We believe that developing highly specific SIRT1 activators, identifying predictive biomarkers, and elucidating tissue-selective regulatory mechanisms can amplify SIRT1's protective effects in cardiac diseases. Current and future clinical trials should establish the safety and efficacy of SIRT1-targeted therapies at the earliest possible stage.

BackgroundThe non-invasive characterization of the tumor microenvironment (TME) is essential for stratifying non-small cell lung cancer (NSCLC) patients who may benefit from immunotherapy. This study investigates a novel approach by integrating dual-energy CT (DECT) parameters with radiomics to quantitatively assess stromal fibrosis (via α-SMA area) and CD8 + T-cell infiltration.MethodsIn this prospective study, 70 treatment-naive NSCLC patients were enrolled. Preoperative DECT scans were used to extract both DECT parameters and radiomics features. Corresponding surgical specimens were analyzed to determine the area percentage of α-SMA-positive stroma and the density of CD8 + T cells, with patients classified into high and low groups for each biomarker. After feature selection, models were constructed based on DECT parameters alone, radiomics features alone, and a combined feature set. Models were evaluated via 5-fold cross-validation.ResultsFor predicting high α-SMA expression, the integrated model combining DECT parameters and radiomics features demonstrated superior performance (AUC: 0.766) compared to models using either modality alone (DECT AUC: 0.670; radiomics AUC: 0.703). In contrast, for predicting CD8 + T-cell density, the DECT-only model (AUC: 0.715) performed comparably to the radiomics model (AUC: 0.695), with no significant gain from integration. Key discriminating features, such as normalized iodine concentration for α-SMA and spectral slope of K40-70 for CD8+, showed significant intergroup differences and plausible biological correlations.ConclusionThe integration of DECT and radiomics presents a feasible, non-invasive strategy to assess specific TME components in NSCLC, underscoring the complementary value of different imaging data types towards developing biomarkers for personalized oncology.

Myocardial infarction (MI) remains a leading cause of global morbidity, often progressing to irreversible ischemic cardiomyopathy due to the limitations of current pharmacological interventions in arresting adverse remodeling. Here, we combined whole-transcriptome sequencing with bioinformatic prioritization in a murine MI model to identify circClint1 as a pivotal, upregulated mediator within the infarcted microenvironment. Mechanistically, luciferase reporter assays and RNA pull-down confirmed that circClint1 functions as a competitive endogenous RNA (ceRNA) for miR-378b, thereby sequestering the miRNA and preventing the targeted degradation of its downstream effector, NPDC1. Notably, both in vivo Western blot and immunofluorescence revealed that ischemic stress triggers a dramatic and spatiotemporal accumulation of NPDC1 protein, particularly within the cytoplasm of peri-infarct cardiomyocytes. Functionally, we established an AAV9-mediated myocardial-specific overexpression model to evaluate the pathological consequences of sustained NPDC1 elevation. Our results demonstrated that NPDC1 accumulation significantly exacerbates post-infarction damage by promoting TUNEL-positive cardiomyocyte apoptosis, intensifying fibrotic remodeling, and impairing the myocardial microcirculation. Conversely, siRNA-mediated genetic silencing of NPDC1 in HL-1 cardiomyocytes effectively attenuated hypoxia-induced oxidative stress, preserved mitochondrial membrane potential, and improved cell viability. Collectively, this study provides definitive evidence that the circClint1/miR-378b/NPDC1 axis is a master detrimental driver of post-MI progression. By elucidating the multi-dimensional role of NPDC1 in coordinating cell death and impaired revascularization, our findings identify this axis as a promising therapeutic target for mitigating myocardial injury and improving long-term cardiovascular outcomes.

The pathogenesis of cancer represents a multifaceted, progressive process driven by an intricate interplay of physical, chemical, biological, and other etiological factors. Recent advancements in clinical oncology, including targeted therapy, surgical resection, radiation therapy, chemotherapy, and immunotherapy, have substantially improved patient outcomes. Targeted therapy has emerged as a promising approach due to its precision and minimal adverse effects. Pyruvate kinase M2 (PKM2) is a metabolic enzyme with protein kinase function that has been extensively studied for its critical role in inflammation and metabolic diseases. By interacting with key oncogenic signaling pathways, PKM2 exerts a critical influence on cancer progression, thereby establishing its status as a potential therapeutic target for cancer. Notably, the role of PKM2 in cancer is not determined solely by expression level but also depends on post-translational modifications, conformational plasticity, nuclear localization, and tumor microenvironment. Extensive preclinical studies have demonstrated that various natural products and compounds exert antitumor effects by modulating PKM2 activity and expression, conformation, or nuclear localization. However, these strategies have not yet entered the clinical trial phase, and the path to clinical application remains fraught with challenges, including the biological complexity of PKM2, tumor resistance, and drug specificity. In summary, this article summarizes the regulatory network between PKM2 and oncogenic signaling pathways, highlights the importance of PKM2 in current clinical strategies for cancer treatment, and discusses the challenges facing therapies targeting PKM2 as well as future research directions.

Liver fibrosis is a common response to chronic liver injury due to multiple etiologies and plays a crucial in the progression of chronic liver disease to cirrhosis, hepatocellular carcinoma, and other liver-related clinical outcomes. Currently, available treatments to block liver fibrosis are designed to eliminate the underlying causes of liver disease. The lack of truly effective drugs to regress or reverse fibrosis is a major unmet clinical need. In this context, this article briefly describes the pathological process of hepatic fibrosis and focuses on reviewing the progress of clinical studies on mechanism-based anti-fibrotic drug development and therapy, highlighting that the positive effect of thyroid hormone receptor-β (THR-β) analogs, fibroblast growth factor 21 (FGF21) analogues, Glucagon-like peptide 1 receptor (GLP-1R) agonists, pan-peroxisome proliferator-activated receptor (pan-PPAR) agonists, fatty acid synthase (FASN) inhibitors, and hydronidone in reducing liver fibrosis caused by specific etiologies. Moreover, multi-pathway guided combination therapy or traditional Chinese medicine demonstrate significant advantages in combating liver fibrosis. Finally, new technologies and approaches affecting the clinical development of anti-hepatic fibrosis drugs were discussed.

Salvia miltiorrhiza (Danshen in Chinese) is a traditional medicinal plant with an extensive range of cardiocerebrovascular protective effects widely used in China and other Asian countries. Danshensu (DSS) is the most important water-soluble component of Danshen and has significant antioxidant, anti-inflammatory, antiplatelet aggregation, antitumor, and other pharmacological activities. However, DSS has poor fat solubility and is unstable due to its o-phenol hydroxyl and α-hydroxy carboxylic acids. Therefore, it is necessary to develop new DSS derivatives through reasonable structural modifications to obtain new drugs with better activity, preferable stability, and higher bioavailability. Our team has previously investigated the effect of Danshen on chronic diseases. Through nearly two decades of research, we have made considerable research progress on the impact of DSS derivatives on cardiocerebrovascular diseases. Based on the published literature and our previous work, it was confirmed that DSS derivatives have a wide range of cardiocerebrovascular protective and other pharmacological effects. Here, this review summarized recent research progress on DSS derivatives in terms of design, synthesis, pharmacological effects, and molecular mechanisms to provide new insights for further research.

PURPOSE:Sepsis-associated encephalopathy (SAE) is a diffuse central nervous system dysfunction that occurs during sepsis. Morin has anti-inflammatory and antioxidative effects. The role of morin in SAE is unclear. METHODS:For in vivo experiments, a SAE mouse model was constructed by cecal ligation and perforation (CLP). The mice were treated using morin and erastin (ferroptosis agonist). The Morris water maze was chosen to examine cognitive function. The mouse hippocampus was collected for HE staining, ELISA, RT-qPCR, western blot, and transmission electron microscopy. For in vitro experiments, HT22 cells received LPS to construct a SAE cell model. The cells were treated with morin, erastin and EX527 (SIRT1 inhibitor) and collected for CCK8 assay, ELISA, western blot and immunofluorescence analysis. RESULTS:In vivo experiments showed that morin ameliorated cognitive dysfunction, hippocampal pathological damage, peripheral inflammation and neuroinflammation in SAE mice. Morin raised the level of SLC7A11, GPX4, FTH1 and GSH, while decreased the level of ACSL4, MDA and iron in SAE mice. Morin also alleviated CLP-induced mitochondrial damage. Erastin diminished the protective effects of morin on SAE mice. In vitro experiments demonstrated that morin alleviated LPS-induced HT22 cell damage and inflammation. Erastin and EX527 reversed the effects of morin on HT22 cells. EX527 additionally reversed inhibitory effect of morin on ferroptosis in HT22 cells. CONCLUSION:Morin alleviates SAE by inhibiting ferroptosis via SIRT1.

ABSTRACT:As a psychoactive drug, marijuana is used for recreational purposes. Given its addictive nature and the serious damage it causes to both individual health and social stability, marijuana has been banned in most countries worldwide. In recent years, with the continuous improvement of basic research, researchers have discovered the role of cannabinoids, the primary active ingredient in marijuana, in multiple human systems. Research found that cannabinoids can regulate immune system function and have therapeutic potential in immune system-related diseases. However, the use of cannabinoids still poses certain hazards. For instance, cannabinoids can exert certain impacts on fetal nervous system development; cannabinoids use can lead to adverse reactions such as dizziness, nausea, and dry mouth. Moreover, there are still numerous contradictions in current research on the effects of cannabinoids, and the mechanisms by which cannabinoids exert protective effects in certain diseases remain unelucidated. In this review, we systematically discuss the endocannabinoid system and summarize the molecular and cellular bases of cannabinoid function in the immune system, and elucidate the effects of cannabinoids on immune system-related diseases.

Sarcopenia, a condition associated with aging, involves progressive loss of muscle mass, strength, and function, leading to impaired mobility, health, and increased mortality. The underlying mechanisms remain unclear, which limits the development of effective therapeutic interventions. Emerging evidence implicates chronodisruption as a key contributor to sarcopenia, emphasizing the role of Bmal1, a circadian clock gene critical for muscle integrity and mitochondrial function. In a skeletal muscle-specific and inducible Bmal1 knockout model (iMS-Bmal1-/-), we observed hallmark features of sarcopenia, including disrupted rhythms, impaired muscle function, and mitochondrial dysfunction. Exercise and melatonin treatment reversed these deficits independently of Bmal1. Building on these findings, the present study elucidates several mechanisms underlying these changes and the pathways by which melatonin and exercise exert their beneficial effects. Our findings indicate that iMS-Bmal1-/- mice exhibit reduced expression of satellite cell and muscle regulatory factors, indicating impaired muscle regeneration. While mitochondrial respiration remained unchanged, notable alterations in mitochondrial dynamics disrupted mitochondria in skeletal muscle. In addition, these mice showed alterations in muscle energy metabolism, compromised antioxidant defense, and inflammatory response. Remarkably, exercise and/or melatonin successfully mitigated these deficits, restoring muscle health in Bmal1-deficient mice. These findings position exercise and melatonin as promising therapeutic candidates for combating sarcopenia and emphasize the need to elucidate the molecular pathways underlying their protective effects.

BACKGROUND:Sepsis is currently one of the leading causes of morbidity and mortality worldwide. Myocardial injury is the most common and severe complication of sepsis. Lactic acid bacteria are a type of gram-positive bacteria found in fermented foods. Our research group previously isolated two new strains G8 and G11 from Jiangshui. METHODS:The probiotic effects of G8 and G11 strains were measured using acid and bile salt resistance tests, bacteriostasis tests, and extracellular polysaccharide (EPS) production tests. In a mouse SIMI model induced by cecal ligation and puncture (CLP), their protective effects were explored using survival rate, body weight, sepsis score, and rectal temperature. Furthermore, RNA-seq and some molecular biology methods were used to investigate G11's protective mechanism against SIMI. RESULTS:Initially, strain G8 and G11 from LAB were successfully isolated and found to possess multiple probiotic functions, such as cholesterol degradation, bacteria inhibition, and production of extracellular polysaccharides (EPS). Treatment with G11 increased the survival rate in CLP-injured mice. Subsequently, G11 treatment improved the rectal temperature, sepsis score, blood routine parameters, and blood biochemical parameters in CLP-injured mice. Additionally, G11 was observed to significantly alleviate cardiac dysfunction, oxidative stress, apoptosis, mitochondrial dysfunction, and inflammation in CLP-injured mice. Finally, this study also confirmed that the AMPK/ACC and SIRT1/PGC-1α signaling pathways may play a crucial role in the protective effects of G11. CONCLUSION:These findings support G11 as a potential cardioprotective probiotic for alleviating SIMI in clinical practice and expanding the use of G11 in sepsis treatment.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Myocardial injury is a common complication in sepsis patients, which accelerates the progression of sepsis, leading to multiple organ dysfunction and poor prognosis. However, there are still many uncertainties about the characteristics, pathogenesis, treatment, and prognosis of sepsis-induced myocardial injury. While modern medical approaches dominate current clinical management of sepsis-induced myocardial injury, emerging evidence highlights the growing therapeutic potential of traditional Chinese medicine in this field, driven by advances in biomedical research. The integration of these two paradigms holds promise for elucidating the pathophysiological mechanisms and identifying novel therapeutic targets for sepsis-induced myocardial injury, which may accelerate the development of innovative treatment strategies. Therefore, this review comprehensively summarizes the pathogenesis and therapeutic interventions of sepsis-induced myocardial injury from both modern medicine and traditional Chinese medicine perspectives, and critically analyzes the two aiming to provide a valuable reference for researchers' understanding of sepsis-induced myocardial injury.